An E mu-v-abl transgene elicits plasmacytomas in concert with an activated myc gene.

摘要: To clarify how the v-abl oncogene of Abelson murine leukemia virus contributes to lymphoid tumorigenesis, we introduced gene linked an immunoglobulin heavy chain enhancer (E mu) into mouse germline. Although development was not detectably affected in young E mu-v-abl mice, three transgenic lines shared a high predisposition develop clonal plasmacytomas that secreted IgA or IgG. The unexpected absence pre-B lymphomas suggests generates such tumors by infecting early progenitor cell has yet activated enhancer. Most bore rearranged c-myc gene, apparently as result spontaneous translocation Igh locus. Moreover, progeny cross with analogous mu-myc mice rapidly developed oligoclonal plasmacytomas. Thus, collusion is stage specific, efficiently transforming plasma cells but B cells.